Synaptic hyperinnervation can be produced in brainstem noradrenergic (NE) neurons, providing an opportunity to study both the physiological consequences of increased synaptic density and the processes controlling collateral sprouting. The trigeminal motor nucleus (MoV) has a rich NE innervation which increases two-fold on more following neonatal 6-OHDA treatment. MoV has few, if any, interneurons, and its cells can be antidromically identified by stimulating nerves supplying the muscles of mastication. Stimulation of NE axons ending in MoV greatly facilitates the jaw-closing reflex initiated by monosynaptic muscle spindle afferent (Ia) fibers. This facilitation is due to an increase in the amplitude of the Ia afferent EPSP. Intracellular recording experiments are described to determine whether the enlarged EPSPs are due to increased numbers of synapses, increased release of transmitter, or increased sensitivity of receptors in the postsynaptic membrane. It will also be determined if forebrain masticatory control regions in the motor cortex an amygdala are facilitated by NE hyperinnervation of MoV. The hypothesis that hyperinnervation represent a conservation of total terminal arborization in a neuron with damaged distant axons (the "pruning effect") will be tested in lateral tegmental NE cells resistant to 6-OHDA damage. Receptor assays and autoradiographs of I125 Alpha1 and Beta receptor ligands will be quantitatively analyzed in normal and hyperinnervated rats to determine whether postsynaptic adrenergic receptors in motor neurons are transported to the neuromuscular junction. These studies will address questions related to the physiologic mechanisms and trophic changes involved in the facilitation of motor neurons hyperinnervated by NE axons.